A Primer on Stroke Prevention and Treatment E-Book

• Herausgeber: John Wiley & Sons
• Kategorie: Fachliteratur
• Sprache: Englisch

Seitenzahl: 638

Veröffentlichungsjahr: 2011

Beschreibung

Society-sanctioned guidelines are valuable tools, but accessing key information can be a daunting task. This book illuminates a clear path to successful application of the American Heart Association/American Stroke Association guidelines. Organized for fast reference, this new volume helps practitioners improve patient care.

Leseprobe

Contents

Contributors

Preface

Classification of Recommendations and Level of Evidence

Part I Overview Topics

1 Stroke Epidemiology George Howard and Virginia J. Howard

Stroke mortality and its disparities

Stroke risk factors

The projected future burden of stroke on the healthcare system

2 Stroke Systems Soojin Park and Lee H. Schwamm

Discussion

A model for stroke systems

Defining the components of the ideal stroke system

Seven stroke system components

Examples of regional stroke systems and state legislative efforts

Conclusion

Gaps in current knowledge

3.Primordial and Primary Prevention of Stroke Nikolaos I.H. Papamitsakis and Robert J. Adams

Primary stroke prevention: a primer

Primordial prevention

What is the risk of a first stroke?

Stroke risk factors

4.Treatment of Patients with Acute Ischemic Stroke Harold P. Adams, Jr.

Introduction

An integrated approach to treatment of acute ischemic stroke

Clinical presentations of acute ischemic stroke

Evaluation of a patient with ischemic stroke

General emergency management

Emergency treatment of the acute ischemic stroke itself

General treatment after admission to the hospital

5.Intracerebral Hemorrhage Opeolu Adeoye and Joseph P. Broderick

Emergency evaluation and diagnosis of intracerebral hemorrhage (ICH)

Treatment of acute ICH/IVH

Prevention of deep vein thrombosis and pulmonary embolism

Recurrent ICH

ICH related to anticoagulation and fibrinolysis: management of acute ICH and restarting antithrombotic therapy

ICH related to fibrinolysis

Surgical treatment of ICH/IVH

Minimally invasive surgery

Early clot evacuation

Withdrawal of technological support

Prevention of recurrent ICH

6  Subarachnoid HemorrhageJonathan L. Brisman and Marc R. Mayberg

Introduction and definitions

Epidemiology, risk factors, and genetics

Imaging characteristics

Diagnosis of IAs

Management of ruptured aneurysms

Acute management

Repair of cerebral aneurysms: microsurgical clipping and endovascular coiling

Comparing outcomes for clipping and coiling

In-hospital care and complications

Neurological complications

Medical complications

Management of unruptured aneurysms

Management of brain AVMs

Gaps in current knowledge

Future directions

7.Prevention of Recurrent Ischemic Stroke

Introduction

Hypertension

Dyslipidemia

Diabetes mellitus

Lifestyle modification

Tobacco use

Alcohol consumption

Obesity

Physical activity

Carotid atherosclerotic disease

Intracranial stenosis

Antithrombotic therapy

Cardioembolic strokes

Non-cardioembolic strokes

Conclusion

8.Post-Stroke Rehabilitation and Recovery Pamela Woods Duncan, Danielle Blankenship, and Nicol Korner-Bitensky

Introduction and background

Recommendations for post-acute stroke rehabilitation and recovery

Management of the consequences of stroke

Patient example, continued: best practice assessments, interventions, and plans

Acknowledgement

Part II Special Topics

9 Stroke in WomenCheryl D. Bushnell

Epidemiology of stroke in women

Evaluation of stroke in women

Secondary prevention of stroke in women

Risk factors for stroke in women

Guidelines for cardiovascular disease prevention in women

Gender differences in post-stroke recovery and treatment

Depression

10 Stroke in Black Patients Fernando D. Testai and Philip B. Gorelick

Introduction

Descriptive epidemiology

Risk factors

Stroke subtypes

Vascular cognitive impairment (VCI)

Stroke severity and recovery from stroke

Clinical trials and barriers to participation

11 Stroke in Children Gabrielle A. deVeber

Discussion

Management

Gaps in current knowledge

Future directions

12 Coagulopathy and Stroke Mark Chan, Richard C. Becker, Svati H. Shah, and Steven R. Levine

Discussion

The evolution of coagulation

von Willebrand Factor (vWF)

Fibrinolytic system proteins

Venous thrombotic disorders

Relationship between arterial and venous thrombosis risk

13 Genetics of Stroke Natalia Rost and Jonathan Rosand

Introduction

The genetic architecture of cerebrovascular disease

Case studies

Conclusion

Acknowledgements

14.Surgical and Interventional Treatment for Carotid Disease Kumar Rajamani and Seemant Chaturverdi

Introduction

CEA for symptomatic carotid stenosis

Which patients benefit most from CEA?

CEA for asymptomatic carotid stenosis

Conclusions

15. Intracranial Atherosclerosis Farhan Siddiq, Burhan Z. Chaudhry, and Adnan I. Qureshi

Introduction

Incidence of intracranial stenosis and atherosclerosis

Risk factors for intracranial stenosis and atherosclerosis

Mechanism of ischemic events associated with intracranial stenosis and atherosclerosis

Risk of recurrent ischemic events associated with intracranial stenosis and atherosclerosis

Evaluation and detection of intracranial stenosis or atherosclerosis

Antiplatelet treatment of intracranial stenosis or atherosclerosis

Anticoagulation for intracranial stenosis or atherosclerosis

Other medical therapies for intracranial stenosis or atherosclerosis

Surgical treatment of intracranial stenosis or atherosclerosis

Endovascular treatment of intracranial stenosis or atherosclerosis

Summary of clinical studies evaluating primary angioplasty for intracranial stenosis

Summary of clinical studies evaluating stent placement for intracranial stenosis

Comparative role of primary angioplasty versus stent placement for intracranial stenosis

Recommended indications from professional organizations

Regulatory approvals, the FDA, and the Centers of Medicare and Medicaid Services (CMS)

Future directions

16 Patent Foramen Ovale Marco R. Di Tullio and Shunichi Homma

Introduction

Frequency of PFO in the general population

Detection of PFO

PFO, ASA, and risk of ischemic stroke

PFO and risk of stroke in the general population

Summary

17 Vascular Cognitive Impairment José G. Merino and Vladimir Hachinski

Introduction

Etiology and pathophysiology

Diagnosis

Treatment

Conclusion

18 Stroke Outcome AssessmentsLinda Williams

Introduction

Types of stroke outcome measures

Disability scales

HRQL scales

Global outcome scales

Analysis of stroke outcome measures in clinical trials

Conclusion

Other Statements Published in 2008

Index

COI Table

This edition first published 2009, © 2009 American Heart Association

American Heart Association National Center, 7272 Greenville Avenue, Dallas, TX 75231, USA

For further information on the American Heart Association:

www.americanheart.org

Blackwell Publishing was acquired by John Wiley & Sons in February 2007. Blackwell’s publishing program has been merged with Wiley’s global Scientific, Technical and Medical business to form Wiley-Blackwell.

Registered office: John Wiley & Sons Ltd, The Atrium, Southern Gate, Chichester, West Sussex, PO19 8SQ, UK

Editorial offices: 9600 Garsington Road, Oxford, OX4 2DQ, UK

The Atrium, Southern Gate, Chichester, West Sussex, PO19 8SQ, UK

111 River Street, Hoboken, NJ 07030-5774, USA

For details of our global editorial offices, for customer services and for information about how to apply for permission to reuse the copyright material in this book please see our website at www.wiley.com/wiley-blackwell

The right of the author to be identified as the author of this work has been asserted in accordance with the Copyright, Designs and Patents Act 1988.

All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, except as permitted by the UK Copyright, Designs and Patents Act 1988, without the prior permission of the publisher.

Wiley also publishes its books in a variety of electronic formats. Some content that appears in print may not be available in electronic books.

Designations used by companies to distinguish their products are often claimed as trademarks. All brand names and product names used in this book are trade names, service marks, trademarks or registered trademarks of their respective owners. The publisher is not associated with any product or vendor mentioned in this book. This publication is designed to provide accurate and authoritative information in regard to the subject matter covered. It is sold on the understanding that the publisher is not engaged in rendering professional services. If professional advice or other expert assistance is required, the services of a competent professional should be sought.

The contents of this work are intended to further general scientific research, understanding, and discussion only and are not intended and should not be relied upon as recommending or promoting a specific method, diagnosis, or treatment by physicians for any particular patient. The publisher and the author make no representations or warranties with respect to the accuracy or completeness of the contents of this work and specifically disclaim all warranties, including without limitation any implied warranties of fitness for a particular purpose. In view of ongoing research, equipment modifications, changes in governmental regulations, and the constant flow of information relating to the use of medicines, equipment, and devices, the reader is urged to review and evaluate the information provided in the package insert or instructions for each medicine, equipment, or device for, among other things, any changes in the instructions or indication of usage and for added warnings and precautions. Readers should consult with a specialist where appropriate. The fact that an organization or Website is referred to in this work as a citation and/or a potential source of further information does not mean that the author or the publisher endorses the information the organization or Website may provide or recommendations it may make. Further, readers should be aware that Internet Websites listed in this work may have changed or disappeared between when this work was written and when it is read. No warranty may be created or extended by any promotional statements for this work. Neither the publisher nor the author shall be liable for any damages arising here from.

Library of Congress Cataloging-in-Publication Data

A primer on stroke prevention and treatment : an overview based on AHA/ASA guidelines / edited by Larry B. Goldstein. p. ; cm.

Includes bibliographical references.

ISBN 978-1-4051-8651-3

1. Cerebrovascular disease. I. Goldstein, Larry B. II. American Heart Association. III. American Stroke Association.

[DNLM: 1. Stroke–prevention & control–Practice Guideline. 2. Stroke–therapy–Practice Guideline. WL 355 P9537 2009]

RC388.5.P6785 2009

616.8′105–dc22

2008051435

ISBN: 9781405186513

Preface

The American Stroke Association/American Heart Association Guidelines are intended to distill a vast amount of information to support the practice of evidence-based medicine. Ye t clinical guideline statements can be a challenge to use and apply in routine practice. In addition, patients are often encountered for whom the available guidelines do not seem to apply directly.

The development of practice guidelines is only one step in the process of improving clinical care. The American Stroke Association/American Heart Association is dedicated not only to increasing knowledge related to stroke and cardiovascular diseases but also to translating the best available science in a way that informs and improves the health and outcomes of both patients and the general public. This book is intended to help bridge the gap between guidelines and practice.

The book is divided into two sections. Chapters in the first section deal with general issues, and those in the second section with focused topics. Each chapter’s major points are highlighted in a bullet point table. To provide clinical context, each chapter begins with a patient example that is referred to in the subsequent discussion. Some chapters use several illustrative cases. The ASA/AHA guidelines are referenced wherever applicable; however, clinical issues not covered in available guidelines are also reviewed. Although taking a clinical perspective, each chapter is thoroughly referenced, providing helpful content for both generalists and stroke specialists.

Clinicians think in terms of people, not guidelines. By example, the approach taken in this book should serve to help providers integrate the information provided in the ASA/AHA guidelines into their practices to the betterment of their patients.

Larry B. Goldstein, MD, FAAN, FAHA

Professor of Medicine Duke University

Medical Center

Durham, NC

Contributors

Harold P. Adams, Jr., MDDirector of the Division of Cerebrovascular DiseasesDepartment of NeurologyCarver College of MedicineUniversity of IowaIowa City, IA, USA

Robert J. Adams, MS, MDStroke CenterMedical University of South CarolinaCharleston, SC, USA

Opeolu Adeoye, MDAssistant ProfessorDepartments of Emergency Medicine andNeurosurgeryUniversity of CincinnatiCincinnati, OH, USA

Richard C. Becker, MDProfessor of MedicineDivisions of Cardiology and HematologyDuke University School of MedicineDuke Clinical Research InstituteDurham, NC, USA

Danielle BlankenshipDoctor of Physical Therapy DivisionDepartment of Community and Family MedicineDuke UniversityDurham, NC, USA

Jonathan L. Brisman, MDDirector, Cerebrovascular and Endovascular NeurosurgeryWinthrop University HospitalLong Island, NY, USA

Cheryl D. Bushnell, MD, MHS Associate Professor, Department of Neurology Wake Forest University Health Sciences Medical Center Boulevard Winston-Salem, NC, USA

Joseph P. Broderick, MD Professor and ChairDepartment of Neurology UC Neuroscience Institute University of Cincinnati Cincinnati, OH, USA

Mark Chan, MDResearch FellowDuke Clinical Research InstituteDurham, NC, USA

Seemant Chaturvedi, MD, FAHA, FAANProfessor of NeurologyStroke Program and Department of NeurologyWayne State UniversityDetroit, MI, USA

Burhan Z. Chaudhry, MD Zeenat Qureshi Stroke Research Center Department of Neurology University of Minnesota Minneapolis, MN, USA

Gabrielle A. deVeber, MD Director, Children’s Stroke Program Division of Neurology Hospital for Sick Children Toronto, Ontario, Canada

Pamela Woods Duncan PhD, PT, FAPTA, FAHAProfessor and Bette Busch Maniscalco Research FellowDoctor of Physical Therapy DivisionDepartment of Community and Family MedicineDuke UniversitySenior FellowDuke Center for Clinical Health Policy ResearchDurham, NC, USA

Philip B. Gorelick, MD, MPHJohn S. Garvin Professor and HeadDirector, Center for Stroke ResearchDepartment of Neurology and RehabilitationSection of Cerebrovascular Disease andNeurological Critical CareUniversity of Illinois College of Medicine at ChicagoChicago, IL, USA

Vladimir Hachinski, MD, DSc, FRCP (C)Distinguished University Professor and Professor of NeurologyUniversity of Western OntarioLondon, ON, Canada

Shunichi Homma, MDMargaret Milliken Hatch Professor of MedicineDivision of CardiologyColumbia UniversityNew York, NY, USA

George Howard, DrPHProfessor and ChairDepartment of BiostatisticsSchool of Public HealthUniversity of Alabama at Birmingham1665 University BoulevardBirmingham, AL, USA

Virginia J. Howard, PhD Research Assistant Professor Department of Epidemiology School of Public Health University of Alabama at Birmingham Birmingham, AL, USA

Nicol Korner-Bitensky, PhD, OTMcGill UniversityFaculty of Medicine, School of Physical and Occupational TherapyCentre de recherche interdisciplinaire en réadaptation du Montréal métropolitain CanadianStroke Network (Theme – Rehabilitation)CanDRIVE – Keeping Safe Older Drivers DrivingMontreal, QC, Canada

Steven R. Levine, MDProfessor of NeurologyDirector, Cerebrovascular Education Program Stroke CenterThe Mount Sinai School of MedicineNew York, NY, USA

Marc R. Mayberg, MDDirector, Seattle Neuroscience InstituteSwedish Medical CenterSeattle, WA, USA

José G. Merino, MD, MPhil Medical DirectorSuburban Hospital Stroke Program Bethesda, MD, USA

Nikolaos I.H. Papamitsakis, MD Director, Stroke Service Assistant Professor of Neurology Medical University of South Carolina Charleston, SC, USA

Soojin Park, MD Massachusetts General Hospital Boston, MA, USA

Adnan I. Qureshi, MD Zeenat Qureshi Stroke Research Center Department of Neurology University of Minnesota Minneapolis, MN, USA

Kumar Rajamani, MDStroke Program and Department of NeurologyWayne State UniversityDetroit, MI, USA

Jose G. Romano, MDAssociate Professor of NeurologyDirector, Cerebrovascular DivisionUniversity of Miami Miller School of MedicineMiami, FL, USA

Jonathan Rosand, MD, MScDepartment of Neurology and Center for Human Genetic ResearchMassachusetts General HospitalProgram in Medical and Population GeneticsBroad Institute of MIT and HarvardBoston, MA, USA

Natalia Rost, MDMassachusetts General Hospital and Center for Human Genetic ResearchProgram in Medical and Population GeneticsBroad Institute of MIT and HarvardBoston, MA, USA

Ralph L. Sacco, MD, MS, FAAN, FAHAChairman of NeurologyOlemberg Family Chair in Neurological DisordersMiller Professor of Neurology, Epidemiology, and Human GeneticsNeurologist-in-Chief, Jackson Memorial HospitalUniversity of Miami Miller School of MedicineMiami, FL, USA

Lee H. Schwamm, MD Massachusetts General Hospital Boston, MA, USA

Svati H. Shah, MDAssistant Professor of MedicineDivision of CardiologyDuke Center for Human GeneticsDuke University School of MedicineDurham, NC, USA

Farhan Siddiq, MDZeenat Qureshi Stroke Research CenterDepartment of Neurology University of Minnesota Minneapolis, MN, USA

Fernando D. Testai, MD, PhDNeurology Clinical InstructorDepartment of Neurology and RehabilitationSection of Cerebrovascular Disease and Neurological Critical CareUniversity of Illinois College of Medicine at ChicagoChicago, IL, USA

Marco R. Di Tullio, MD Professor of Medicine Division of Cardiology Columbia University New York, NY, USA

Linda Williams, MDChief of Neurology, Roudebush VAMCResearch Coordinator, VA Stroke QUERIAssociate Professor, NeurologyIndiana UniversityBloomington, IN, USA

Classification of Recommendations and Level of Evidence

Reference is made throughout this book to ASA/ AHA Guideline recommendations. The scheme is summarized in the table and serves as a reference for the reader’s interpretation of both estimates of certainty of treatment effects (i.e., Level A, B, or C) and the magnitude of that effect (Class I, IIa, IIb, and III). It should be noted that in this scheme, Class III reflects a treatment for which the risk generally outweighs its benefit. The table also provides phrases that are generally used to reflect the strength of a recommendation.

Applying Classification of Recommendations and Level of Evidence

Part I Overview Topics

1 Stroke Epidemiology

George Howard and Virginia J. Howard

EXAMPLE CASE

A 45-year-old right-handed African-American man examination is notable only for a right upper-motor residing in central North Carolina has a history of neuron pattern facial paresis and 3/5 strength in his hypertension and presents with right-sided weakness right arm and leg with depressed right-sided deep without a language impairment and visual or sensory tendon reflexes and a right plantar-extensor deficits. He also has a 50-pack-year history of response. A brain CT scan obtained 4 hours after cigarette smoking. His examination revels a body symptom onset was normal. An EKG followed by a mass index (BMI) of 35, a blood pressure of transthoracic echocardiogram showed left ventricular 180/95 mm Hg, a regular pulse, no cervical bruits, hypertrophy (LVH). and no cardiac murmur. His neurological examination is notable only for a right upper-motor neuron pattern facial paresis and 3/5 strength in his right arm and leg with depressed right-sided deep tendon reflexes and a right plantar-extensor response. A brain CT scan obtained 4 hours after symptom onset was normal. An EKG followed by a transthoracic echocardiogram showed left ventricular hypertrophy (LVH).

MAJOR POINTS

Although overall stroke mortality rates have been rapidly declining, consistently higher rates remain among African-Americans (particularly between ages 45 and 65) and Southerners.Risk factors influencing stroke incidence can be stratified into two tiers:

         Tier 1. Risk factors consistently identified as playing a major role

      The big three risk factors contributing over half of the population attributable risk: hypertension, diabetes, and smoking

      Others: left ventricular hypertrophy, atrial fibrillation, and heart disease

         Tier 2. Risk factors likely playing a role

      Risk factors for risk factors: obesity, fat distribution, and physical activities may have minor direct impact but play a major role by increasing the risk for hypertension and diabetes (tier 1 factors)

      Risk factors important to control regardless of direct stroke risk: dyslipidemia and metabolic syndrome

      Risk factors playing an important role in special populations: asymptomatic carotid stenosis, postmenopausal hormone therapy, and sickle-cell disease

      Risk factors likely playing a smaller or questionable role.

The graying of America is likely to have a major impact on the absolute number of stroke events in the next half-century, with an anticipated dramatic increase in the number of stroke events particularly among elderly women.

Stroke mortality and its disparities

There are few US national data describing stroke incidence, and as a result, most of what is known about stroke epidemiology focuses on mortality rates. The age–sex-adjusted stroke mortality rates by race-ethnic group for the United States between 1979 and 2005 are shown in Figure 1.1. This figure reflects the remarkable successes and failures in stroke. During this brief 26-year period, stroke mortality has declined by 48.4% for African-Americans, by 52.9% for whites, and by 45.5% for other races [1] – a decline in a chronic disease that is simply striking. Along with similar reductions in heart disease mortality, this decline was acknowledged as one of the “Ten Great Public Health Achievements” of the 20th century (the only two achievements that were listed for a specific disease) [2].

This same figure, however, underscores one of the great failures in the 20th century – striking disparities by race. Using the year 2000 age standard, in 1979, African-Americans had an age-adjusted stroke mortality rate that was 30.8% higher than whites, whereas other races had a rate that was 26.7% below whites. This is in contrast to 2005, when African-Americans had stroke mortality rates 43.0% higher than whites, a relative increase of 39.6% ([43.0– 30.8]/30.8) in the magnitude of the racial disparity in stroke deaths. This increase in stroke mortality among African-Americans persists despite the Healthy Persons 2010 goals (one of the guiding documents for the entire Department of Health and Human Services) having as one of its two primary aims “to eliminate health disparities among segments of the population, including differences that occur by gender, race or ethnicity, education or income, disability, geographic location, or sexual orientation” [3].

This figure obscures another disturbing pattern. The African-American–white differences in stroke mortality rates are three to four times (300–400%) higher between the ages of 40 and 60. These are attenuated with increasing age to become approximately equivalent above age 85 (see Figure 1.2)[4]. Data from the Greater Cincinnati/Northern Kentucky Stroke Study suggest that this excess burden of stroke mortality is primarily attributable to higher stroke incidence rates in African-Americans (rather than case fatality), and is uniformly shared between first and recurrent stroke, as well as between isch-emic and hemorrhagic (both intracerebral and sub-arachnoid) stroke subtypes; all have incidence race ratios between 1.8 and 2.0 [5,6].

Another great disparity in stroke mortality is the “stroke belt” – a region in the southeastern United States with high stroke mortality that has persisted since at least 1940 (see Figure 1.3 [7]). Whereas the overall magnitude of geographic disparity is between 30% and 50%, this map shows that specific regions (such as the “buckle” region of the stroke belt along the coastal plain of North Carolina, South Carolina, and Georgia) have stroke mortality rates well over twice those of other regions. There are as many as 10 published hypothesized causes of this geographic disparity [8,9], but the reason for its existence remains uncertain. Finally, depending on sex and age strata, the magnitude of the southern excess stroke mortality is between 6% and 21% greater for African-Americans than for whites [10]. The example patient is at a higher risk of stroke and stroke mortality compared with Americans of other race-ethnic groups because he is an African-American and because he resides within the stroke-belt region of the country.

Fig. 1.1   Age-adjusted (2000 standard) stroke mortality rates for ages 45 and older, shown for African-American, white, and all other races. Data were retrieved from the Centers for Disease Control Wonder System [1], with ICD-9 codes 430–438 for years 1979–1998, and ICD-10 codes I60 to I69 for years 1999–2005.

Fig. 1.2   African-American-to-white age-specific stroke mortality ratio for 2005 for the United States [4].

Fig. 1.3  Geographic pattern of stroke mortality rates between 1991 and 1998 for US residents aged 35 and older. Centers for Disease Control and Prevention, Stroke Atlas. www.cdc.gov/DHDSP/library/maps/strokeatlas/index.htm.

Stroke risk factors

The current American Heart Association/American Stroke Association Primary Stroke Prevention Guidelines provides a comprehensive review of potential stroke risk factors with an extensive listing of references (offering a total of 572) [11]. A list of more than 30 separate risk factors and conditions reviewed in these guidelines is summarized in Table 1.1, along with classifications on the support for treatment and the level of evidence regarding the role of the factor in modifying stroke risk. Although the table is comprehensive, the goal of this section is to provide a more focused discussion within a framework that may be quickly considered by practicing clinicians. Any attempt to reorganize the listing provided in the guidelines should not be interpreted as minimizing the importance of any factor in an individual patient, but rather as helping to set priorities in a resource-limited environment.

The foundation of the approach to organize risk factors is to consider efforts to establish “risk functions” for stroke in which the factors are considered as independent predictors of stroke risk taken from the more comprehensive list. Although reported over 15 years ago, the most well known of these risk assessments is from the Framingham Study cohort in which independent stroke predictors included age, systolic blood pressure, use of antihypertensive medications, diabetes mellitus, current smoking, established coronary disease (any one of myocardial infarction [MI], angina or coronary insufficiency, congestive heart failure, or intermittent claudica-tion), atrial fibrillation, and LVH [12]. It is striking that this list of independent predictors was confirmed by perhaps the second best known of these risk functions, produced from the Cardiovascular Health Study, which included precisely the same list of risk factors (plus additional measures of frailty) [13]. Not accounting for age as a disease risk factor and considering systolic blood pressure and use of antihypertensive medications as one factor, that these two risk functions were concordant with the independent risk factors for stroke strongly suggests these six factors as “first-tier” risk factors for stroke (see Table 1.2). The example patient has a history of hypertension, an additional, modifiable, “first-tier” stroke risk factor.

Table 1.1 Summary of recommendations from the American Heart Association Guidelines for primary stroke prevention

Nonmodifiable  1  Age  2 Sex  3  Low birth weight  4 Race ethnicity  5  Genetic factors (IIb, C)Well-documented and modifiable risk factors  1  Hypertension (I, A)  2  Cigarette smoking (I, B)  3  Diabetes (I, A)  4  Atrial fibrillation (I, A)  5  Other cardiac conditions   •  Left ventricular hypertrophy (IIa, A)   •  Heart failure (IIb, C)  6  Dyslipidemia (I, A)  7  Asymptomatic carotid stenosis (I, C)  8  Sickle-cell disease (I, B)  9  Postmenopausal hormone therapy (III, A)  10  Diet and nutrition   •  Sodium intake (I, A)   •  Healthy diet (DASH) (I, A)   •  Fruit and vegetable diet (IIb, C)  11  Physical inactivity (I, B)  12  Obesity and body fat distribution (I, A)Less well-documented or potentially modifiable risk factors  1  Metabolic syndrome (see individual components)  2  Alcohol abuse (IIb, B)  3  Drug abuse (IIb, C)  4  Oral contraceptive use (III, B/C)  5  Sleep-disordered breathing (IIb, C)  6  Migraine (ratings not provided, but considered “insufficient” to recommend a treatment approach)  7  Hyperhomocysteinemia (IIb, C)  8  Elevated lipoprotein (a) (IIb, C)  9  Elevated lipoprotein-associated phospholipase A2 (absence of evidence)  10  Hypercoagulability (absence of evidence)  11  Inflammation (IIa, B)  12  Infection (absence of evidence)  13  Aspirin for primary stroke prevention (III, A)

DASH, Dietary Approaches to Stop Hypertension

Attempts were made to classify each potential risk factor on two scales (shown in the table as Roman numerals and letters). First, each was classified by the strength of evidence for a treatment approach into strata: I) conditions for which there is evidence for and/or general agreement that the procedure or treatment is useful and effective; IIa) conditions for which there is conflicting evidence and/or a divergence of opinion about the usefulness/efficacy of a procedure or treatment, but the weight of evidence or opinion is in favor of the procedure or treatment; IIb) conditions for which there is conflicting evidence and/or a divergence of opinion about the usefulness/efficacy of a procedure or treatment, and the usefulness/efficacy is less well established by evidence or opinion; and III) conditions for which there is evidence and/or general agreement that the procedure or treatment is not useful/effective and in some cases may be harmful. The second classification was on the level of evidence into strata: A) data derived from multiple randomized clinical trials; B) data derived from a single randomized trial or nonrandomized studies; or C) consensus opinion of experts.

The “population attributable risk” (the proportion of stroke events attributable to specific risk factors) is a product of both the magnitude of the impact of a risk factor and its prevalence in the at-risk population, and provides important insights to the contributions of these first-tier risk factors. The population attributable risk for major stroke types was recently reported from the Atherosclerosis Risk in Communities Study (Figure 1.4)[14] showing that the combination of hypertension, diabetes, and cigarette smoking contributes the great majority of risk for lacunar (82%), nonlacunar (58%), and car-dioembolic (73%) stroke. The substantial contribution of these three risk factors to stroke risk is underscored by the population attributable risk in the American Heart Association (AHA)/American Stroke Association (ASA) guidelines paper [11], which, while based on different studies, sums to more than 100% (i.e., more than 100% of the risk of stroke is attributed to different causes). The guidelines statement suggests that hypertension alone contributed between 30% and 40% of stroke risk, cigarette smoking between 12% and 18%, and diabetes between 5% and 27% [11]. Clearly, these three risk factors could be called “the big three” of the first tier. In addition to being an African-American residing in the stroke belt with a history of hypertension, the example patient smokes cigarettes, further increasing his stroke risk. His clinical syndrome is consistent with a “lacunar” syndrome.

Table 1.2 A proposed structure for consideration for modifiable stroke risk factors

1 First-tier factors  •  The “big three” factors (based on population attributable risk)   a.   Hypertension   b.  Diabetes   c.  Cigarette smoking  • Other first-tier factors   a.  Heart diseases   b.  Atrial fibrillation   c.  Left ventricular hypertrophy2 Second-tier factors  • Risk factors for risk factors. Examples:   a.  Obesity and body fat distribution   b.  Physical inactivity  • Risk factors important to control (regardless of stroke risk).     Examples:     a.  Dyslipidemia     b.  Metabolic syndrome  • Risk factors important in special populations     a.  Asymptomatic carotid stenosis     b.  Postmenopausal hormone therapy     c.  Sickle-cell condition • Risk factors with a smaller effect or questionable effect (others)

Fig. 1.4  Population attributable risk for major stroke subtypes of stroke from the Atherosclerosis Risk in Communities study for the “big three” risk factors and all others (including second-tier risk factors). Adapted from data available in Ohira et al. [14].

Fig. 1.5  Awareness, treatment, and control of blood pressure.CHS, Cardiovascular Health Study; NHANES, National Health and Nutrition Examination Survey; REGARDS, Reasons for Geographic and Racial Differences in Stroke.

As a clinician, it is not only important to treat specific risk factors in individual patients, but it is also important to think at the level of a group of patients (e.g., a practice) and allocate resources where they can have the greatest impact. Importantly, treatment approaches that will lead to substantial reductions in the overall burden of stroke would need to particularly target this “big three” cluster of risk factors. Although there have been some improvements in their management over time, the control of these risk factors remains sub-optimal. For example, awareness, treatment, and control of high blood pressure in the National Health and Nutrition Examination Survey (NHANES) Study over the period 1988–1991 to 1999–2000, and from the Reasons for Geographic and Racial Differences in Stroke Study through 2003–2005, are shown in Figure 1.5 [15]. These data suggest that while there may have been an increase in awareness of hypertension from 70% to 90%, an increase in treatment from 52% to 80%, and an increase in control (to systolic blood pressure < 140 and diastolic blood pressure < 90) from 25% to 52%, approximately 50% of hypertensive individuals still fail to achieve control of their condition. Likewise, while there were substantial decreases in the prevalence of cigarette smoking from 1965 (with a prevalence of 51.2% in men and 33.7% in women) to 1990 (with a prevalence of 28.0% in men and 22.9% in women), the rate of decline substantially slowed in the 16 years between 1990 and 2005. The prevalence only decreased to 23.4% in men and to 18.3% in women – with one in every five adults remaining as active smokers [16]. We are also largely failing at adequate control of diabetes, for which between 35% and 50% of type 2 diabetics in the NHANES study had hemoglobin A1c values at or above 8% [17]. Although we know that impacting these “big three” risk factors would reduce stroke incidence by more than 50%, interventions to manage these risk factors are not being optimally employed.

The other three “first-tier” risk factors – history of heart diseases, atrial fibrillation, and LVH – are as important (or perhaps even more important) in individual patients with these prevalent conditions [12,13]. The population prevalence of each of these conditions is lower, thereby making their overall contributions smaller. Also, it is clear that effective treatments exist for high-risk patients with atrial fibrillation using warfarin [18–20], although the standard treatments for LVH and previous heart disease are more complex. Hence, it could be suggested that a primary care physician could have the largest impact intervening on the “big three,” but the awareness and treatment of individual patients who have these “other first-tier” risk factors remain important. The example patient also had LVH, possibly related to his history of hypertension.

Although non-first-tier risk factors should not be thought of as being unimportant, it is useful to use a different framework for their consideration. This framework includes thinking about these “other” risk factors in three classes.

There are several risk factors that do not directly impact stroke risk, but rather act as risk factors for one or more of the first-tier risk factors. For example, obesity is largely absent or has a relatively minor role in multivariable stroke risk models. In the Framing-ham and other studies, obesity is a potent risk factor for diabetes and carries an odds ratio 2.5 times greater for incident diabetes among participants with a BMI of 30 or greater [21]. In the Incidence of Hypertension in a French Working Population (IHPAF) study, obesity was the single greatest predictor of incident hypertension; individuals with a BMI above 30 had an odds ratio for incident hypertension 5.5 times greater for men and 2.8 times greater for women [22]. With obesity playing such a major role on the risk for two of the three “first-tier” stroke risk factors (and also having a relationship with atrial fibrillation and LVH), its absence in the major risk models should not be interpreted as reflecting a lack of importance, but rather as identifying obesity prevention and treatment as a point of intervention to reduce the major risk factors for stroke. A similar argument could be made for other non-first-tier stroke risk factors, most notably physical inactivity. The example patient had a BMI in the obese range – a factor that increased his chances of developing hypertension.

There are other non-first-tier risk factors for which treatment is critical for reasons that extend quite beyond protection from stroke. Examples of this class include treatments for dyslipidemia. With statin treatment, patients with coronary heart disease or additional risk factors such as hypertension or diabetes not only have a reduction in their risk of coronary heart events, but also a reduction in the risk of a first stroke [11]. In the Stroke Prevention by Aggressive Reduction in Cholesterol Levels (SPARCL) trial that assessed statin treatment for secondary stroke prevention among stroke/transient ischemic attack patients with a low-density lipopro-tein level between 100 and 190 mg/dL, there was a 48% reduction (hazard ratio [HR] of 0.58) for subsequent coronary events in addition to a 16% reduction (HR of 0.84) in stroke events [23]. While in SPARCL there were more stroke than MI events, in most populations, the incidence of MI overwhelms that of stroke, and the impact of statin treatment is more powerful for coronary event prevention – suggesting that individuals with elevated lipid levels should be treated with statins almost regardless of their stroke risk. The interpretation of the role of the metabolic syndrome, a clustering of other well-documented cardiovascular risk factors, may also fall to this consideration.

There are also risk factors in special populations. For example, it is clear that surgical treatment of individuals with asymptomatic carotid disease will reduce stroke risk if the operation is performed safely; however, it is not clear whether (a) this is a risk factor for stroke or part of the causal pathway (i.e., hypertension and diabetes cause advancement of atherosclerosis that in turn causes stroke) and (b) treatment is warranted given the relatively small absolute risk reduction [24]. This is reviewed in the chapter on carotid surgery. A similar “special population” is the use of postmenopausal hormone therapy, which has been shown in three randomized trials to be associated with higher cardiovascular risk (including stroke) [25–27]. In all three of these studies, however, the risk of placing women on hormone therapy appeared to be associated with an early higher risk of thrombotic events, raising the question of the optimal treatment for women already on such treatment (who have already passed this high-risk period).

A number of other risk factors discussed in the AHA/ASA Primary Prevention Guideline have been documented in individual studies as potentially related to increased stroke risk [11]. Although their role in increasing stroke risk may be relatively smaller, and additional information may be needed to better understand their roles, the treating physician should be aware of each and consider them for treatment.

The projected future burden of stroke on the healthcare system

As noted earlier, the decline in stroke mortality, presumed to be at least partially attributable to declines in stroke incidence, has been a striking success [2]. Even assuming a continued decline in stroke incidence (perhaps a bold assumption), these declines are likely to be overwhelmed by the “graying of America” as reflected in the population pyramids shown in Figure 1.6. The year 2000 pyramid makes the “baby-boomer” bulge at approximately 45 years apparent – and it is noteworthy that this bulge is at the age when stroke risk is frequently considered to increase. Between 2000 and 2050, it is anticipated that the overall US population will grow by approximately 48% [28]. This “baby-boomer” bulge suggests that there will be a 109% growth among individuals aged 60–69, a 100% growth for individuals aged 70–79, a 196% growth for individuals aged 80–89, and a remarkable 569% growth for individuals over 90 [29]. With the risk of stroke approximately doubling with each increasing decade of age, these increases in the elderly population are likely to lead to more than a doubling in the number of stroke events before 2050 [30]. This increase in the number of persons having strokes, particularly among Hispanic and African-American populations, has been estimated to be associated with public health costs in excess of $2.2 trillion dollars over this period – $1.52 trillion for non-Hispanic whites, $313 billion for Hispanics, and $379 billion for African-Americans [30]. Unfortunately, the graying of America makes it likely that the absolute numbers of Americans having and being disabled by stroke will be increasing.

The example patient’s stroke may have largely been preventable. Although he was an African-American residing in the stroke belt, lifestyle changes such as smoking cessation and weight loss would have lowered his risk. Effective control of his blood pressure would also be important as the stroke that occurred can be attributed to occlusion of a small intracranial artery, which is particularly sensitive to the effects of hypertension.

References available online at www.wiley.com/go/strokeguidelines.

Fig. 1.6 Population pyramids for the United States in the year 2000 (left) and in the year 2050 (right).

2

Stroke Systems

Soojin Park and Lee H. Schwamm

EXAMPLE CASES

Case 1

A 61-year-old white male arrived at a 120-bed community and regional teaching hospital at 11:30 pm, with left-sided weakness and right-gaze preference. His family insisted he was completely normal at 10:30 pm (1 hour earlier) when, as they were finishing dinner, they witnessed him develop these symptoms. Emergency medical services (EMS) were called and the patient was brought by ambulance to this hospital, which was the nearest one with an emergency department (ED). He was examined by the ED physician who estimated his National Institutes of Health Stroke Scale (NIHSS)score to be 23; he had occasional respiratory pauses and was subsequently intubated for an unenhanced computed tomography (CT) scan of the brain. The radiologist’s dictation read “dense middle cerebral artery (MCA) sign on the right and subtle ischemic changes.”

The neurologist on call for the ED was contacted by telephone and was apprised of the following additional history. The patient had atrial fibrillation and had been on warfarin for stroke prevention until a month ago, when he had a gastrointestinal hemorrhage requiring admission but no blood transfusions. A colonoscopy during that admission revealed two polyps, which were felt to be the cause of bleeding, and were removed. Three days after the colonoscopy, he restarted warfarin. Two weeks after restarting warfarin, when a little blood was noted in his stool, he was instructed to discontinue warfarin until a follow-up appointment could be arranged. After learning the additional history, the neurologist recommended admission and advised against IV thrombolysis (IV tissue-type plasminogen activator [tPA]) because of the bleeding risk and because he felt that the NIHSS score was “too high.” The neurologist planned to see the patient in the morning because he was not an IV tPA candidate.

The ED physician phoned the acute stroke service at a nearby tertiary care hospital for a second opinion at 11:55 pm. After reviewing the elements of the ED physician’s examination in detail, the acute stroke physician estimated the NIHSS at 18. Without being able to view the CT images that were described over the telephone as having “subtle ischemic changes,” the stroke physician felt uncomfortable recommending IV tPA. The patient’s family was concerned and requested transfer to the tertiary care hospital in order to have the opportunity to be enrolled in an acute care clinical trial or be screened for endovascular treatment. Because the NIHSS by itself was not considered to be a contraindication for IV or intra-arterial (IA) therapy, the patient was transported by helicopter. On arrival, he was intubated with persistent chemical paralysis and sedation required for the helicopter transport. CT angiogram was performed as soon as the patient arrived at 4:30 am, 5 hours after the onset of symptoms. The CT angiography revealed an occlusion of the right internal carotid artery and an evolving infarction in the entire MCA and anterior cerebral artery distributions with no visible collaterals. Due to the presence of completed infarct on CT, no endovascular therapy was recommended. Of note, bilateral aspiration pneumonia was visualized on CT.

Early hemicraniectomy was considered and discussed with the family, emphasizing the possibility of reduced mortality without any expected early improvement in the stroke symptoms, but the family declined the intervention. The patient was transferred to the neurointensive care unit, where he was closely monitored overnight. Within 36 hours, despite aggressive medical measures to treat malignant cerebral edema, the patient died as a result of transtentorial herniation.

Case 2

A 51-year-old woman with a history of hypothyroidism and tobacco dependence described the onset of language difficulty and right-sided weakness at 9:45 pmafter getting out of the bath. She had no symptoms at 9:00 pm when her boyfriend last saw her, but when she called a friend at 10:00 pm, she was difficult to understand on the telephone. EMS was called, and the ambulance was routed past a nearby hospital to be brought to the nearest state designated stroke center at 10:45 pm. Because of the prearrival notification by EMS, the CT scan technologist was alerted and was holding open a CT scanner for the patient when she arrived. On examination at the hospital’s ED, she was noted to have right-sided weakness and aphasia. Her blood pressure was 150/80 mm Hg, and her pulse was regular at 80 bpm. There was no evidence of acute aortic dissection, myocardial ischemia, hypoglycemia, or comorbid terminal illness. She was not taking any aspirin or prescription medications.

An unenhanced head CT was interpreted as showing no mass lesion, bleeding, or clearly visible new infarction. The ED physician’s assessment was that this patient might be a potential IV tPA candidate. Rather than trying to transfer the patient prior to treatment to the nearest comprehensive stroke center (40 miles away), they contacted the stroke center for a telemedicine-enabled stroke (telestroke) consultation at 11:00 pm, 2 hours after she was last known to be well.

The telestroke consultation was initiated, and the diagnosis was felt to be acute ischemic stroke, with ischemia likely in the left MCA territory. An NIHSS score performed over interactive videoconferencing was 9. After the patient’s history and CT images were reviewed by the telestroke consultant, it was agreed that the patient should receive IV tPA, and together, they reviewed with her family the risks and benefits, calculated the dose, and supervised its administration. The IV tPA bolus was given at 11:30 pm, 2.5 hours after she was last seen well. She was then transferred to the regional stroke center.

Her neurological condition improved en route, and by the time she arrived, she had only a mild right pronator drift and right facial weakness. She had an magnetic resonance imaging (MRI) with magnetic resonance angiography (MRA) of the head and neck and magnetic resonance perfusion imaging. There were several cortical foci of restricted diffusion-weighted imaging in the left MCA territory, one in the left middle frontal gyrus, one in the frontal operculum, one in the precentral gyrus, and one in the postcentral gyrus, consistent with acute ischemia. A region of abnormality on perfusion-weighted MRI with prolonged relative mean tissue transit time and reduced relative cerebral blood flow was centered in the left frontal operculum, considerably larger in size than the patient’s focal area of restricted diffusion in this location. MRA identified a dissection in the left cervical internal carotid artery. She was discharged on a 3-month course of warfarin anticoagulation. The patient recovered fully and returned home after 4 days in the hospital.

MAJOR POINTS

A systems-based approach to stroke care delivery is needed to increase access to limited stroke resources and eliminate geographic and financial disparities.Telemedicine technology and air medical transport can help collapse the barriers of time and distance between patients and stroke expertise to facilitate rapid delivery of thrombolytic therapy or other advanced interventions.Systematic implementation of guideline-based care is essential, and providers should focus on delivering to these interventions in each domain of the stroke care continuum.Stroke care systems should strive to address the consensus recommendations contained in the Stroke Systems of Care framework, and should focus not just on the individual domains but also on the linkages between the discrete domains of care.Lessons can be learned from other successful disease centered systems of care delivery such as the trauma and acute cardiac systems of care.Whenever possible, objective and verifiable criteria should be used to establish hospitals’ acute stroke capability and stroke center status, and this information should be made publicly available.Continuous quality improvement activities and evaluation should occur within each domain and the stroke system of care model itself should be subject evaluation and modification over time.Gaps in knowledge exist and further research is needed to identify the best methods to measure the effectiveness of systems of care implementation, and to refine the elements necessary within each domain. Legislation efforts and strong financial incentives will likely be needed to make significant improvements.

Discussion

Acute care demands on general neurologists are rising as geography, practice environments, and reimbursement issues contribute to disparities in acute stroke coverage (Figure 2.1). These two cases demonstrate how access to stroke expertise and treatment options can differ based on different practice environments, financial incentives, and manpower constraints. In the absence of an organized stroke system of care, centers of excellence can be surrounded by other centers struggling to provide even rudimentary stroke services. The advent of organized networks of prehospital care coupled with stroke centers, as well as the utilization of new technology such as telemedicine, increases access to specialty acute care for those who would not have otherwise received opportunities for thrombolytic therapy or other advanced interventions. The old paradigm of preliminary evaluation over several hours in a small community hospital ED, followed by transfer to a tertiary center after the window for intervention had expired (a “drift and shift” approach), is being gradually replaced by rapid evaluation and initial administration of therapeutics in consultation with expert centers prior to transfer (the “drip and ship” approach).

A stroke system strives to ensure a more equitable distribution of scarce resources. Within any one community, there are often too many urgent needs, and not enough qualified healthcare providers to meet them. Not all hospitals need to possess all capabilities. Because patients arriving at hospitals with acute stroke within the 3-hour time window (generally within 2 hours of symptom onset) is a low-frequency, high-impact event, and because half of all strokes result in minimal disability (NIHSS score <4), which generally does not require thrombolytic intervention, acute stroke expertise on-site may not be practical. Strategies such as telemedicine or air medical transport that can bring patients and providers together rapidly and efficiently may help reduce disparities in access to acute stroke care. Coordinated approaches to addressing the acute stroke needs of an entire state or region are best pursued in the context of a stroke systems of care framework that engages key stakeholders and forges links between the different critical components of care delivery.

Fig. 2.1 Relationship between stroke mortality and distribution of neurologists based on the Centers for Disease Control and Prevention’s Online Atlas of Stroke Mortality (http://apps.nccd.cdc.gov/giscvh2/Select2Maps.aspx,).

A model for stroke systems

The trauma system is a successful model from which useful parallels for stroke care may be drawn. A trauma system is a network involving all phases of patient care – starting from injury prevention, to the scene of injury, through the trauma center, recovery, and rehabilitation. Putting in place a trauma system, or improvements in an aspect of a trauma system, is associated with improved hospital survival among the seriously injured [1]. Within a region, there is a hierarchy of centers based on demonstrated need in the community, the capability to provide care to the seriously injured, and a predetermined expectation of proper coordination and rapid transportation of the most seriously injured from less capable to tertiary care centers. Trauma systems strive to provide similar coverage between urban and rural communities within a region.

The potential to improve stroke outcomes by focusing on building infrastructure and systems of care was recognized early in the stroke center movement. While a standardized approach to hospital-based stroke care had been evolving, innovative programs in prehospital EMS, community education, and rehabilitation were being developed in isolation. There was a clear need for a more integrated approach to address the disparities in care delivery and access observed throughout the United States and within smaller regions (e.g., cities, counties, states).

Defining the components of the ideal stroke system

The American Stroke Association’s (ASA) Task Force on the Development of Stroke Systems examined ongoing stroke initiatives in the United States (publications from 1994 to 2003) and drafted the Recommendations for the Establishment of Stroke Systems of Care in 2005 [2]. The recommendations were organized by the seven components that an ideal stroke system would address (Table 2.1), elaborating on the prior concept of the chain of stroke survival, which was organized based on the temporal sequence of acute stroke care. The Task Force recommendations offered a set of guiding principles for state and regional collaboratives that were developing their own stroke systems of care, with an emphasis on providing maximal access to care to the greatest number of individuals, rather than carving out special or unique populations of patients based on corporate affiliations or hospital financial interests. The Task Force provided strategies to overcome barriers and acknowledge key shared goals.

Table 2.1 Seven components that an ideal stroke system should address (adapted from the American Stroke Association’s Recommendations for the establishment of Stroke Systems of Care 2005) [2]

1 Primordial and primary prevention 2 Community education 3 Notification and response of emergency medical services 4 Acute stroke treatment 5 Subacute stroke treatment and secondary prevention 6 Rehabilitation 7 Continuous quality improvement activities within each domain and across the system itself

Seven stroke system components

Primordial and primary prevention

Improving systems to detect and treat disease earlier will help decrease death, disability, and costs associated with untreated disease. Primordial prevention refers to strategies designed to prevent or minimize the development of the intermediate disease states that are themselves risk factors for stroke (e.g., smoking, obesity prevention, and control). It is, essentially, primary prevention of the diseases or risk factors that increase the risk of stroke. Primary prevention of stroke refers to treatment of already established diseases in the population (e.g., hypertension, atherosclerosis, diabetes) to reduce the risk of stroke. This topic will be covered in more detail in Chapter 3.

Heart disease and stroke share many common risk factors; partnering with other stakeholders improves the chances of adequate funding for prevention programs and research. The American Cancer Society, the American Diabetes Association, and the American Heart Association (AHA) published a joint scientific statement pledging their common goals in 2004 [3]. The Center for Disease Control set Healthy People goals for 2010, which included a reduction of death from heart disease and stroke by 25% (these goals were met earlier than expected in 2008) [4].

Community education

Within a stroke system, it is important to develop initiatives to enhance public knowledge and awareness in collaboration with key community partners so as to maximize the cultural appropriateness and effectiveness of the message. Shared goals include education regarding the signs and symptoms of stroke and stroke risk factors, and reinforcing the appropriate use of EMS for patients or bystanders who note the onset of stroke symptoms. The general public’s knowledge of stroke symptoms has been dangerously inadequate [5–10]. While traumatic injury is readily apparent, stroke symptoms and their significance can be more difficult to appreciate and do not consistently trigger notification of EMS.

Historically, the public’s knowledge of stroke has lagged behind the knowledge of heart disease [6,11]. The AHA/ASA views public education as a vital component of its mission.

Notification and response of EMS

A multidisciplinary expert panel convened by the ASA addressed the role of EMS systems in the wider stroke system of care (Table 2.2) [12]. Key goals, barriers, potential solutions, and appropriate measurement parameters were identified.

Among the recommendations were universal access and coverage for enhanced 911 (land and wireless) services for all callers in all geographic areas covered by the relevant stroke system of care.

Table 2.2 Adapted from the American Stroke Association (ASA) Panel on emergency medical service systems (EMSS) role in the wider stroke system of care [12]

1 Universal access and coverage for enhanced 911 services 2 Pivotal role of EMSS communicators 3 Prioritization of acute stroke in dispatch guidelines 4 American Heart Association/ASA-approved caller interrogation tools 5 Statewide emergency stroke system protocols 6 Measure and share key process measures for continuous quality improvement

They emphasize the pivotal role played by EMS communicators, as they are the first point of contact for the patient, family, and EMS responder. EMS communicators, by recognizing stroke symptoms and triaging appropriately, hold the power to prime the stroke system to efficiently and expertly care for an acute stroke patient. Therefore, it is critical to provide accurate and frequent education on the recognition of stroke symptoms. The challenges inherent in this task vary distinctly with geography (e.g., rural, urban, proportion of population with limited English-language skills) and are hampered by a lack of national standards for the equitable coordination and delivery of emergency medical care [13].

EMS dispatch guidelines should be reorganized to require that acute stroke patients be assigned to the highest priority response. The use of AHA/ASA-approved caller interrogation tools is recommended to help EMS communicators to identify suspected stroke patients accurately and to err on the side of “over-triage” so as to minimize the risk of false-negative assessments.

Until statewide emergency stroke system protocols are universal, regions should be responsible for coordinating local transport protocols and emphasizing transport to the nearest designated stroke center, even if efforts are sometimes at odds with geopolitical forces. Issues of ambulance ownership and scarcity of resources in certain communities offer a special challenge for stroke systems to provide adequate coverage and opportunities for acute care.

For the purposes of continuous quality improvement (CQI), it is vital that data reflecting key process measures are recorded and shared in a useful way. Data should be collected and analyzed both at an individual EMS transactional level as well as a regional aggregate to influence behavior and improve quality. Analysis of the time intervals between contact with an EMS dispatcher, EMS dispatch, scene arrival, and hospital arrival may help develop strategies to reduce delays and direct patients’ triage appropriately.

Air transport may be more efficient than ground transport if it is initiated quickly [14–17]. At the same time, in the face of the rising costs of health care, specific indications for initiating air transport should be analyzed on a regional basis. Geospatial characteristics of the region should be taken into account [18] as well as the realistic likelihood of arrival at destination within a treatable time window. Given the complex nature of air transport, most patients transported by helicopter or fixed wing aircraft would not arrive at a stroke center in time to receive IV tPA, unless the helicopter were to be dispatched directly to the scene, as is done in some communities for acute trauma. In most cases, the rationale for air medical transport is access to advanced therapeutics such as catheter-based therapies beyond 3 hours after symptom onset.

Through the use of telemedicine and other strategies to facilitate access to acute stroke expertise, it is feasible to create an environment in which many hospitals can function as “acute stroke capable” centers in which patients can be initially triaged and rapidly assessed. If acute stroke expertise is not consistently available at a given institution, every effort should be made to establish referral relationships with nearby stroke centers, so that patients can be transferred to an appropriate facility for admission after stabilization and possible treatment with IV thrombolysis.

Finally, there will always be hospitals without the infrastructure to care for acute stroke patients, and some patients will still arrive via private car, or be transported by EMS to these facilities when stroke may not be rapidly diagnosed or patients are hemodynamically unstable. These hospitals must still be considered when creating a stroke system of care and EMS triage algorithm, even if they have opted out of the role of being “acute stroke capable” or even providing the basic components of inpatient stroke care. Small size, rural location, or limited resources may compel certain hospitals to routinely transfer their complex stroke patients, or all their stroke patients, to larger, better-resourced facilities. These relationships should be built into the fabric of the system of care, so that the process of rapid evaluation and delivery of care is as seamless as possible for all patients, regardless of their geographic or economic circumstance.

Acute stroke treatment

As recently as 12 years ago, ischemic stroke was a syndrome without an acute treatment option, for which management was largely focused on rehabilitation and avoidance of adverse outcomes in the subacute setting. Despite the landmark approval of IV tPA as an acute treatment for ischemic stroke in 1996, administration rates were low. According to regional and nationwide studies (United States and Canada) from 1996 to 2002, only 0.6–8.5% of patients presenting with nonhemorrhagic stroke were being treated with IV tPA [19–23].

The reasons for the low rate of IV tPA administration were probably multifactorial [23,24] (Table 2.3). These included the lack of painful symptoms, impaired communication that often accompanies stroke, the wide variety of possible symptoms, the frequent delays in activating EMS, and the public’s lack of knowledge of stroke symptoms. Studies that have evaluated arrival times suggest that only 17– 35% of stroke patients arrive within the time that allows treatment in the 3-hour window [19,20,22,23]. The lack of an organized infrastructure to rapidly triage and evaluate patients compounds the problem and reduces the likelihood of timely treatment, even where treatment is available. In the presence of these obstacles, and the concerns over malpractice litigation if complications should occur, rates of IV tPA administration have remained low. In studies that delineated reasons for nontreatment of patients arriving within 3 hours, physician-determined contraindications to IV tPA accounted for only 27–52% [19,23].

Interestingly, one center that had participated in the original National Institute of Neurological Disorder and Stroke IV tPA clinical trial [25] achieved a postmarketing administration rate of up to 15% of all ischemic strokes admitted to its hospital [26] (compared with the 0.6–8.5% national rates in the same time period). This center had an established program for prearrival notification of its experienced acute stroke team by EMS. This is one example of how an integrated stroke system of care can contribute to higher rates of acute stroke treatment by linking together different components within the continuum of providers.

Table 2.3 Possible reasons for low administration rates of IV tissue-type plasminogen activator (tPA), 1996–1999

1 Clinicians’ concerns about the efficacy of tPA 2